Tentorial Dural Arteriovenous Fistulas as a Cause of Thalamic Edema: 2 Cases of an Important Differential Diagnosis to Consider

Abstract

The differential diagnosis for bilateral thalamic edema is extensive and includes vascular, neoplastic, metabolic, and infectious causes. Of the vascular causes of thalamic edema, arterial and venous infarctions are well-documented, but dural arteriovenous fistulas (dAVFs) are a relatively uncommon and widely underrecognized cause of thalamic edema. Dural AVFs are notoriously difficult to diagnose clinically, especially in the absence of hemorrhage, and cross-sectional imaging findings can be subtle. This can result in a delayed diagnosis, and occasionally, an invasive biopsy for further clarification of a purely vascular disease. In this review, we detail our experience with the imaging diagnosis of dAVF as a cause of thalamic edema and present a short differential of other vascular causes.

Keywords: delayed diagnosis; dural arteriovenous fistula; tentorial dAVF; thalamic edema; thalamus.

Figure 1.

A 65-year-old man with bithalamic edema from dural arteriovenous fistula (dAVF). A, An axial fluid attenuation inversion recovery (FLAIR) sequence showing expansile signal abnormality in the left greater than right thalamus, with prominent enhancement (B) and no restricted diffusion on the apparent diffusion coefficient (ADC) maps (C). D, An axial FLAIR sequence showing postbiopsy changes in the left thalamus (arrow), which showed reactive changes without evidence of malignancy. E, A time-of-flight magnetic resonance (MR) angiography which showed possible arterialized flow in the straight sinus. F, A lateral view digital subtraction angiography in the late arterialized phase, showing early venous drainage into the vein of Galen related to a dAVF (arrow).

Figure 2.

A 52-year-old man with bithalamic edema from dural arteriovenous fistula (dAVF). A, An axial noncontrast computed tomography (CT) showing edema in both thalami, better depicted on the axial fluid attenuation inversion recovery (FLAIR) sequence (B). There is only mild associated enhancement on the postcontrast sequence (C). D, A sagittal maximum intensity projection image from a CT angiogram showing arterialized flow in the straight sinus. Early to mid arterial phase lateral digital subtraction angiography (DSA) from an internal carotid artery injection shows early venous drainage into the straight sinus (arrow, E). Lateral DSA from the external carotid artery injection more clearly shows early venous drainage into the straight sinus from a dAVF (F).

Figure 3.

Dural sinus thrombosis in a young patient with headaches. A, An axial noncontrast computed tomography (CT) showing edema in the left greater than right thalamus. B, At the level of the corona radiata shows hyperdensity within the straight sinus, concerning for deep venous thrombosis, which was confirmed on subsequent CT venogram (arrow, C).

Figure 4.

Artery of Percheron infarct in an 87-year-old man with altered mental status. A, An axial diffusion-weighted image of the brain showing acute infarcts in both thalami (arrows). B, An axial diffusion-weighted image of the brain at the level of the cerebral peduncles, showing acute infarction of the mid brain (arrow). C, A coronal maximum intensity projection image from a computed tomography angiogram (CTA) performed an hour prior to the magnetic resonance imaging (MRI), showing wide patency of the basilar artery without thrombosis. The distribution of infarcts on MRI and patent basilar artery on CTA are consistent with an artery of Percheron infarct.

Figure 5.

Posterior reversible encephalopathy syndrome (PRES) in a patient with severe hypertension and a history of medical noncompliance. A, Edema in the right greater than left thalamus. Edema is also present in the pons and bilateral cerebellar white matter (B and C, respectively). There was no associated contrast enhancement or restricted diffusion. Vascular imaging did not show dural sinus thrombosis or evidence of arteriovenous shunting or fistula.

Figure 6.

Anoxic brain injury in a 65-year-old found down in cardiac arrest. A, Abnormal fluid attenuation inversion recovery (FLAIR) signal in both thalami, as well as the caudate heads, putamina, and cerebral cortices. Diffusion-weighted imaging (DWI) and ADC maps (B and C) shows associated restricted diffusion in the areas of signal abnormality, consistent with cytotoxic edema.

Figure 7.

Contrast-enhanced magnetic resonance (MR) showing normal intracranial venous anatomy. This is a maximum intensity projection of a sagittal postcontrast image of the brain, depicting the intracranial venous anatomy. The blue arrow is the internal cerebral vein, the arrowhead shows the vein of Galen, the curved arrow shows the straight sinus, the dashed arrow shows the torcular Herophili, the star shows the inferior sagittal sinus, and the double-headed arrow shows the superior sagittal sinus.